scholarly journals Clarithromycin Suppresses Human Respiratory Syncytial Virus Infection-InducedStreptococcus pneumoniaeAdhesion and Cytokine Production in a Pulmonary Epithelial Cell Line

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Shin-ichi Yokota ◽  
Tamaki Okabayashi ◽  
Satoshi Hirakawa ◽  
Hiroyuki Tsutsumi ◽  
Tetsuo Himi ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Cell Line ◽  
Human Respiratory Syncytial Virus ◽  
Receptor Expression ◽  
Host Cells ◽  
Epithelial Cell Line ◽  
Paf Receptor ◽  
Pulmonary Epithelial Cell ◽  
Syncytial Virus

Human respiratory syncytial virus (RSV) sometimes causes acute and severe lower respiratory tract illness in infants and young children. RSV strongly upregulates proinflammatory cytokines and the platelet-activating factor (PAF) receptor, which is a receptor forStreptococcus pneumoniae, in the pulmonary epithelial cell line A549. Clarithromycin (CAM), which is an antimicrobial agent and is also known as an immunomodulator, significantly suppressed RSV-induced production of interleukin-6, interleukin-8, and regulated on activation, normal T-cell expressed and secreted (RANTES). CAM also suppressed RSV-induced PAF receptor expression and adhesion of fluorescein-labeledS. pneumoniaecells to A549 cells. The RSV-inducedS. pneumoniaeadhesion was thought to be mediated by the host cell’s PAF receptor. CAM, which exhibits antimicrobial and immunomodulatory activities, was found in this study to suppress the RSV-induced adhesion of respiratory disease-causing bacteria,S. pneumoniae, to host cells. Thus, CAM might suppress immunological disorders and prevent secondary bacterial infections during RSV infection.

scholarly journals Identification of gene biomarkers for respiratory syncytial virus infection in a bronchial epithelial cell line

2008 ◽  
Vol 2 (3-4) ◽  
pp. 113-125 ◽  
Author(s):  
Yuh-Chin T. Huang ◽  
Zhuowei Li ◽  
Xhevahire Hyseni ◽  
Michael Schmitt ◽  
Robert B. Devlin ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Virus Infection ◽  
Cell Line ◽  
Respiratory Syncytial Virus Infection ◽  
Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
Syncytial Virus

3-Nitrotyrosine attenuates respiratory syncytial virus infection in human bronchial epithelial cell line

2005 ◽  
Vol 288 (5) ◽  
pp. L988-L996 ◽  
Author(s):  
Yuh-Chin T. Huang ◽  
Zhuowei Li ◽  
Luisa E. Brighton ◽  
Johnny L. Carson ◽  
Susanne Becker ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Cell Line ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Bronchial Epithelial ◽  
Viral Particles ◽  
Rsv Infection ◽  
Syncytial Virus

3-Nitrotyrosine (NO2Tyr), an l-tyrosine derivative during nitrative stress, can substitute the COOH-terminal tyrosine of α-tubulin, posttranslationally altering microtubular functions. Because infection of the cells by respiratory syncytial virus (RSV) may require intact microtubules, we tested the hypothesis that NO2Tyr would inhibit RSV infection and intracellular signaling via nitrotyrosination of α-tubulin. A human bronchial epithelial cell line (BEAS-2B) was incubated with RSV with or without NO2Tyr. The release of chemokines and viral particles and activation of interferon regulatory factor-3 (IRF-3) were measured. Incubation with NO2Tyr increased nitrotyrosinated α-tubulin, and NO2Tyr colocalized with microtubules. RSV-infected cells released viral particles, RANTES, and IL-8 in a time- and dose-dependent manner, and intracellular RSV proteins coprecipitated with α-tubulin. NO2Tyr attenuated the RSV-induced release of RANTES, IL-8, and viral particles by 50–90% and decreased α-tubulin-associated RSV proteins. 3-Chlorotyrosine, another l-tyrosine derivative, had no effects. NO2Tyr also inhibited the RSV-induced shift of the unphosphorylated form I of IRF-3 to the phosphorylated form II. Pre-exposure of the cells to NO2(0.15 ppm, 4 h), which produced diffuse protein tyrosine nitration, did not affect RSV-induced release of RANTES, IL-8, or viral particles. NO2Tyr did not affect the potential of viral spreading to the neighboring cells since the RSV titers were not decreased when the uninfected cells were cocultured with the preinfected cells in NO2Tyr-containing medium. These results indicate that NO2Tyr, by replacing the COOH-terminal tyrosine of α-tubulin, attenuated RSV infection, and the inhibition appeared to occur at the early stages of RSV infection.

Respiratory syncytial virus-induced cytokine production by a human bronchial epithelial cell line

1993 ◽  
Vol 265 (5) ◽  
pp. L472-L478 ◽  
Author(s):  
T. L. Noah ◽  
S. Becker
Keyword(s):  
Respiratory Syncytial Virus ◽  
Epithelial Cell ◽  
Cell Line ◽  
Proinflammatory Cytokines ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Cytokine Mrna ◽  
Bronchial Epithelial ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) is the most common cause of lower respiratory infection in infants and young children, but the pathogenesis of RSV-induced inflammation is not well defined. We hypothesized that in vitro infection of a human bronchial epithelial cell line (BEAS) would induce production of proinflammatory cytokines. BEAS cells were infected with RSV, and cells and supernatants were assayed for cytokine mRNA and protein changes at several time points after infection. Cytokine mRNA in BEAS cells was measured by polymerase chain reaction of reverse-transcribed RNA from whole cell lysates; cytokine levels in supernatants were measured by bioassay or immunoassay. Our results indicated that interleukin-5ay or immunoassay. Our results indicated that interleukin-8 (IL-8) was induced at 4 h after infection (during the eclipse phase of RSV infection) with accumulation of IL-8 in supernatants by 24 h after infection. Increased levels of IL-6 and granulocyte macrophage colony-stimulating factor in supernatants were only detected by 96 h after infection, during the RSV replicative phase. Interferon-alpha and -gamma transcripts were not detectable at any time point. We conclude that the effects of RSV on airway inflammation may be at least partly mediated by sequential production of proinflammatory cytokines in infected airway epithelium.

The lack of attachment of transformed embryonic lung epithelial cells to collagen I is corrected by fibronectin and FXIII

1986 ◽  
Vol 86 (1) ◽  
pp. 95-107
Author(s):  
M. Paye ◽  
C.M. Lapiere
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Line ◽  
Lung Epithelial Cells ◽  
Collagen I ◽  
Epithelial Cell Line ◽  
Embryonic Lung ◽  
Lung Epithelial ◽  
Minimal Concentration ◽  
Pulmonary Epithelial Cell

PER cells, a transformed pulmonary epithelial cell line that adhered to a large extent to a fibronectin substratum, were found to be attachment-deficient to collagen I. Although fibronectin can bind to collagen I monomers and polymers, the addition of exogenous fibronectin in the attachment medium induced the adhesion of these cells to collagen I polymers but not to monomers. By adding the transglutaminase of blood coagulation, FXIII, in the presence of fibronectin, the attachment of PER cells to collagen I monomers could be recovered while the minimal concentration of fibronectin needed to promote their adhesion to polymers was lowered. These studies indicate that FXIII enhances the fibronectin-mediated attachment of PER cells to collagen I.

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